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CLIN MED II- ENDOCRINOLOGY > ADRENAL DISORDERS > Flashcards

ADRENAL DISORDERS Flashcards

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1
Q

parts of adrenal gland and what they secrete

A

adrenal medulla- inner 1/4
- secretes catecholamines (epi) in fight or flight

adrenal cortex- outer 3/4
- secretes steroid hormones (aldosterone, androgens/estrogens/progesterone, glucocorticoids–> cortisol)

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2
Q

catecholamines
- primary
- functions

A

Primary
- dopamine, epi, norepi

functions
- inc alertness, transmit nerve impulses in brain
- stim gluconeogenesis, fatty acid release for energy
- dilates bronchioles and pupils
- norepi–> constrict BV, inc BP
- epi—> inc HR and metabolic rate

released in response to stress/triggered by SNS

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3
Q

aldosterone
- secreted from where and when

A

released via RAAS
- dec in MAP bp–> activates aldosterone to inc BP
- triggers inc Na+ reabsorp and K+ secretion in distal tubules+collecting duct

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4
Q

cortisol
- secreted where and when

A

HPA pathway
- CRH—>ACTH—>cortisol
- typically secreted contiunously with diurnal rhythm (peak in morning, diminish overnight, also inc w/stress)

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5
Q

cortisol effects

A

protect against hypoglycemia
- promotes gluconeogenesis
- enhances lipolysis (fatty acid for energy)
- supresses immune system
- reduce circulating calcium

cortisol is catabolic

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6
Q

cushings sydrome v. disease

A

syndrome: sx due to inc cortisol secretion
disease: cushing syndrome + pituitary adenoma (inc ACTH)

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7
Q

cushing syndrome
- causes

A

most to least common (I PASS ALL EXAMS)
- Iatrogenic (prescribed steroids is MCC)
- pituitary tumor (ds, inc ACTH)
- adrenal adenoma or carcinoma
- ectopic ACTH production (SCC, thymoma ca, pancreatic islet ca)

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8
Q

cushing syndrome presentation

A
  • Abd purple striae
  • Bruise easy, poor healing
  • central obesity
  • dorsal fat pad (buffalo hump)
  • ext muscle wasting
  • face round, moon faqce
  • gluc excess
    (ABCDEFG)

MSK- symm weakness proximal U/LE
misc- menstrual changes, dec libido, inc infx, inc glc + BP, dec K+

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9
Q

who do we test for cushing syndrome

A
  • osteoporosis or HTN in young adults
  • multiple features of cushing syndrome
  • adrenal incidentalomas (incidental finding adrenal tumor)
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10
Q

screening for cushings syndrome
- 3 tests

A
  • overnight low dose dexmethasone suppression test (DST)—> ideal first test
  • late night salivary cortisol
  • 24 hr urinary free cortisol excretion (UFC)
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11
Q

cushings

overnight low dose dexamethasone suppression test
- how
- pos result

A
  • admin dexameth at 11 pm, check cortisol at 8 am
  • pos= cortisol>5
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12
Q

cushings

late night salivary cortisol
- how
- pos result

A
  • saliva collected prior to bedtime and cortisol measured
  • ## pos result variable, depends on lab (elevated)
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13
Q

cushings

24 hr urinary free cortisol excretion
- how
- pos result

A
  • collect urine x24 hrs, test for cortisol levels
    -pos = >4x upper limited
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14
Q

cushing syndrome dx
- determine cause w ACTH

A

LOW (<5)–> due to adrenal tumor or hyperplasia
- get CT scan

intermed/high —> additional testing
- see if its pituitary adenoma v. ectopic tumor

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15
Q

cushing syndrome dx
- ACTH intermed/high next steps

A

CRH stim test and HIGH dose dexameth suppression test

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16
Q

cushing syndrome

CRH stim test
- how
- results (AP tumor v. ectopic ACTH tumor)

after finding ACTH levels are intermed/high

A

IV admin CRH
- if ACTH/cortisol level inc + response = AP tumor (cushing ds)
- if ACTH/cortisol level do not respond = ectopic ACTH tumor

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17
Q

cushing syndrome

HIGH dose dexamethasone suppression test
- how
- results

A

used to confirm dx
- administer 8 mg PO dexameth at 11 pm
- check cortisol at 8:30 pm before dosing and 9 am after dosing
- if >50-80% suppression = pos Cushing ds (pit tumor)

ectopic ACTH completely resistant to any feedback inhibition

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18
Q

cushing syndrome IMAGING
- adrenal
- pituitary
- ectopic ACTH producing tumor

A
  • adrenal = CT
  • pituitary = pituitary MRI, if no mass–> petrosal sinus sampling (gold standard for cush ds)
  • ectopic ACTH producing tumor = Ct or MRI
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19
Q

cushing syndrome tx options

A

iatrogenic: glucocorticoid taper

surgical removal
- pit tumor= transsphenoidal surgical removal
- adrenal = adrenalectomy
- ectopic = surgery, chemo/rad
- after removal start steroid taper

if unable to get surgery– ketoconazole, monitor LFTs

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20
Q

why do we do a steroid taper for cushing syndrome

A

to prevent adrenal insufficiency/adrenal crisis

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21
Q

adrenal insufficiency
- define
- types and hormone levels

A

def of adrenal hormones, mainly cortisol (aldosterone can be affected in primary)
- primary (addisons): issue w adrenal gland, cortisol + aldosterone def, ACTH will be high
- secondary: pituitary
- tertiary: hypothalamic

secondary and tertiary cortisol def only

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22
Q

primary adrenal insufficiency causes

Study These Flashcards
A
  • MCC is autoimmune ds
  • infectious ds (TB MCC worldwide), fungal infx, CMV, syph
  • bilat hemorrhagic adrenal infarction
  • metastatic cancer
  • iatrogenic (adrenalectomy, drugs like fluconazole, rifampin)
23
Q

secondary/tertiary adrenal insuff causes

Study These Flashcards
A

secondary
- MCC long term steroid therapy of 2 and 3 degree (sx start when stopped)
- pts recently cured of cushings synd
- pit tumor/mass, irradiation
- sheehan syndrome

tertiary
- long term steroid
- pts cured of cushings
- hypothalamic ds

24
Q

primary adrenal insuff/addisons S/Sx

Study These Flashcards
A
  • hypoglycemia
  • hyperpigmentation (sun tan/bronze over knuckle, elbow, knee, mucosa)
  • GI (n/v, ano, wt loss)
  • neuro (weak, confused)
  • low aldosterone (Low Na, high K, low BP)

sx develop over months/yrs

pigmentation and low aldosterone ONLY in primary

25
adrenal insuff secondary/tertiary presentation
- plasma ACTH low, cortisol deficient (but aldosterone NOT affected) - hypoglycemia, weakness, confusion, n/v/d, wt loss hyponatremia (less common) | NO hyperkalemia, NO hyperpigmentation
26
adrenal insuff dx testing?
check 8 am serum cortisol + plasma ACTH level + perform ACTH stim test
27
adrenal insuff - 8 am serum cortisol and plasma ACTH level results
- low cortisol + high ACTH = primary - low cortisol + low ACTH = secondary or tertiary---> get MRI of brain (pit+hypothal)
28
what test confirms dx adrenal insuff - results
ACTH stim test (gold standard) - admin synth ACTH, check cortisol 30-60 min after - serum cortisol rise to >=18 = nl adrenal func - serum cortisol dec <18 = confirms insufficiency
29
adrenal insuff tx - primary - secondary/tertiary - all - surgery or acute illness
- primary (chronic): daily hydrocortisone or prednisone, +/- fludrocortisone (replaces aldosterone) - second/tertiary: daily hydrocortisone - all: tx underlying ds - surgery or acute illness: double dose steroids to avoid crisis
30
# adrenal insuff adrenal crisis - presentation
Sx of adrenal insuff + progression - dehydration - CV collapse, low BP - severe abd pain - acute renal failure
31
adrenal crisis - precipitating factors - tx
- abrupt cessation of steroids - stress (trauma, infx, surgery) tx - IV hydrocortisone, IV fluid + 5% dextrose - tx triggering condition
32
primary hyperaldosteronism - define
excessive aldosterone indep of RAAS system - inc Na, dec K - fluid retention and HTN
33
primary hyperaldosteronism causes
- MCC bilat adrenal cortical hyperplasia (men 50-60 yo) - adenoma/ Conn syndrome(women 30-50 yo) - adrenal carcinoma
34
primary hyperaldosteronism presentation
- mod-severe persistent HTN (MC FEATURE) - H/A - fatigue - absence periph edema!! - hypokalemia (muscle weakness, paresthesia) ## Footnote suspect in cases of refractory HTN
35
primary hyperaldosteronism dx - screening + result - confirmation + result - subtype classification
screening - ratio of plasma aldosterone to plasma renin - if PAC/PRC >20 = pos confirmation - aldosterone suppression w oral sodium loading - give high salt diet 3 days, measure--> inc urine aldosterone = pos subtype - CT of adrenal to see if adenoma, hyperplasia, or carcinoma
36
who should we screen for primary hyperaldosteronism
- HTN >150/100 on 3 diff days - refractory HTN to tx w 3 agents (or controlled w 4+) - HTN w hypokalemia and not on diuretic tx - personal or FHx of CVA <40 yo - FHX primary hyperaldosteronism
37
primary hyperaldosteronism tx - bilat hyperplasia - adenoma or carcinoma
- bilat hyperplasia : spirinolactone - adenoma (Conns) or carcinoma: surgical resection
38
congenital adrenal hyperplasia
autosomal rec genetic d/o (gene from both parents) - defect in enzyme (21-hydroxylase) that converts cholesterol to cortisol within adrenals - produce too little cortisol and/or aldosterone + TOO MUCH androgen - excess ACTH leads to overstim + hyperplasia
39
classic CAH - when is it dx - untreated complication
severe, life threatening form - dx infancy or childhood - salt wasting (cannot maintain Na in blood---> hyponatremic) - if not tx quickly--> shock, coma, death
40
classic CAH presentation
- virilizing features (abnorm genitalia in females) - emesis, dehydrated, shock - HYPONATREMIA + HYPERKALEMIA (no aldosterone) - hypoglycemia (no cortisol)
41
non classic CAH - when is it dx -
more common/less severe (some enz activity) - dx late childhood/adulthood - no salt wasting - buildup of aldosterone and cortisone precursors---> virilizing features
42
nonclassic CAH presentation
- premature signs of puberty (early) - females--> ambigous genitalia (clitoris enlarged, labial fusion, but nl uterus and ovaries) - males ---> no genital abd, but enlarged penis/scrotum at birth
43
CAH dx and tx (medical and surgical)
Dx - inc 17-hydroxyprogesterone levels in serum tx medical - classic: hydrocortisone + fludrocortisone + salt tabs - nonclassic: hydrocortisone if Sx surgical - early surgical revision female genital abnorm.
44
pheochromocytoma
tumors that produce, store, and secrete catecholamines (dopamine, epi, norepi) - 40% occur part of familial d/o (MEN2, von hippel lindau) - life threatening if un dx
45
pheochromocytoma presentation
sx present in paroxysmal manner triad: (PHE) - palpitations - HA - excessive perspiration additional - HTN, tremor, anxiety, hyperglycemia
46
pheochromocytoma dx
24 hr urinary fractionated catecholamines and metanephrines - if urine pos --> confirm location tumor w imaging (CT/MRI abd + pelvis)
47
pheochromocytoma tx - surgical - medical - other testing
- surgical resection w venous ligation (after med prep) med prep - 2 week before surgery = alpha blocker (phenoxybenzamine) - 2-3 days before surgery = beta blocker (propanolol) if metastatic ds - resect + systemic chemo genetic testing - von hippel lindau, MEN 2, neurofibromatosis type 1 (NF1)
48
adrenocortical carcinoma (ACC) - growth pattern - age affected - hereditary?
rare tumor - aggressive and quickly grow - age <5, 40-50s - sporadic or linked to hereditary cancer syndrome (MEN1)
49
ACC presentation - functional v. silent
functional (pos hormonal activity) - present w cushing syndrome - glucocorticoid excess (wt gain, weak, abnorm fat distribution) silent (no hormonal activity) - present w sx related to tumor growth - abd + flank pain -->then incidental found on imaging
50
ACC dx
CT + MRI abd and pelvis (adenoma v. ACC) FNA cytology to determine if metastatic or primary origin
51
ACC staging 1-4
stage 1- confined to adrenal gland, biggest tumor <5 cm stage 2- same as 1, but tumor size >5 cm w out RFs stage 3- tumor any size + 1 RF (tumor infiltrating surrounding tissue, invasion into vena cava/renal vein, pos LN but no distant metastases) stage 4- distant metastases
52
ACC tx
surgical resection - prior to surgery undergo hormone testing (if cortisol producing tumor requires glucocorticoid post op)
53
adrenal tumors categories
- benign or malignant - functional (hormone secreting) or silent (no hormone activity) most adrenal tumors benign/silent, some benign functional (cushing, pheo, aldosteronism), rare ACC can be functional or silent
54
# adrenal tumors adrenal incidentalomas - define - benign adenoma v. carcinoma/metastases (characteristics)
- mass >1 cm found by chance on imaging eval for: - benign adenoma (homogenous, low density, <4 cm, smooth border) - carcinoma or metastases ( >4 cm, irreg shape, inhomongenous, calcified, necrosis

CLIN MED II- ENDOCRINOLOGY (11 decks)

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